Differential expression of miRNAs in myocardial tissues of rats with lipopolysaccharide- induced endotoxemia.
- Author:
Tao DING
1
;
Yang LI
;
Ruizhu TANG
;
Xuan ZHANG
;
Yu YUN
;
Jian LI
;
Dianhua WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Endotoxemia; metabolism; Injections, Intraperitoneal; Interleukin-1beta; metabolism; Lipopolysaccharides; Male; MicroRNAs; metabolism; Myocardium; metabolism; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Toll-Like Receptor 4; metabolism; Tumor Necrosis Factor-alpha; metabolism; Up-Regulation
- From: Journal of Southern Medical University 2015;35(2):213-217
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo analyze the differential miRNA expression profile in the myocardium of rats with lipopolysaccharide (LPS)-induced endotoxemia and explore the role of miRNA in endotoxin-induced myocardial injury.
METHODSTwenty male SD rats received intraperitoneal injection of 10 mg/kg LPS (n=10) or an equivalent amount of saline solution (n=10). At 24 h after LPS injection, the rats were sacrificed to detect myocardial expressions of TLR4, TNF-α and IL-1β using real-time PCR and for observing myocardial ultrastructures under transmission electron microscopy. The differentially expressed miRNA in the myocardium were detected using a miRNA array, and the common differentially expressed miRNAs were selected for verifying their actual expressions using real-time PCR.
RESULTSTLR4, TNF-α and IL-1β were over-activated in the myocardium of LPS-treated rats, in which mitochondria swelling, structural damaged and cytoplasmic vacuoles were observed. In LPS-challenged rats, miR-194-3p, miR-344a-3p, miR-465-3p, miR-501-5p, miR-3596c, miR-185-3p, and miR-877 were found up-regulated significantly, whereas miR-208b-3p, miR-547-3p, miR-141-3p, miR-28-5p, and miR-3585-5p down-regulated in the myocardium.
CONCLUSIONSignificant differential expression of the miRNAs occurs in the myocardium of LPS-treated rats, suggesting their involvement in endotoxin-induced myocardial injury.